Does Rupp or the Gouchers take thyroid medication?

Hyperthyoridism is not really the subject we are talking about. Everyone on here has so far claimed to have HYPOthyroidism which is much more common including about 20 million diagnosed cases in the US and countless undiagnosed cases. It is much more common than you think.

I agree though that it is odd that this happens in runners more. (at least from what I have seen)

I am no elite runner however, and most of the runners I know with it are not elite. People may be on drugs of some sort, but I don't think this is one you can use for benefits if you are healthy.

unknowingly wrote:

okay,so let me get this straight.....it has to be a life long thing?

okay so diabetics, anyone who uses orthotics, anyone who wears shoes that correct pronation, anyone who has any allergies, etc. They all fall into the same category.

diabetes is a better comparison that orthotics. in diabetes either your body fails to produce enough insulin (Type 1) or your body has a reduced ability to use insulin (Type 2). Type 1s are on insulin their entire life. hypothyroidism is like Type 1 diabetes in that your thyroid stops working as well as it should. Right now, as in Type 1 diabetes, there is no cure for a thyroid that does not fucntion normally. you can only control it with synthetic thyroid hormone.

Hyperthyroidism is relevant in that consuming thyroid hormones unnecessarily results in hyperthyroidism. It will in-turn harm long-term performance.

Some nonelite athletes push themselves hard too. No surprise you know some of them with thyroid problems.

Hypothyroid issues certainly are the most common type. Also the toughest to diagnose.

Surely there are drugs that will enhance endurance - EPO for example. Athletes willing to cheat can do much better than tampering with thyroid hormones.

T3 is what regulates EPO production. T3 is a thyroid hormone.

T3 supplementation - does nothing for you, unless you are hypothyroid

Altitude - does what it does, increases EPO

T3 + Exposure to Altitude = *EPO JACKPOT*

Find the doc who will diagnose the condition and prescribe the >>correct>proper amounts<<, sleep the rewards and it is all technically LEGAL. The LEGAL part is the kicker!

Those are just the facts my naive little friends.

Do the research then get back to us.

Ghost of Brigham Young wrote:

I'm not calling anyone out specifically, then again the incidence of hyperthyroidism is approx 1 in 2,000 or 0.05% or 136,000 people in USA. Clearly the incidence amongst eite American runners is much higher, why, I have no idea. What do YOU think?

OK now falling under the new rules that it has to be lifelong. So like the above poster said if someone wears orthdoics? Watch? Shoes? Oh wait it has to only be availble from a doctor I forgot that new rule... prescription alergy medication, orthodics still, contacts or glasses, physical therapy, gynocology (for women), any type of seeing a general practictioner for regular checkups, anything else? Or are there more new rules?

Correction T3 plays a role in EPO production.

Another type of autoimmune thyroid problem is called a silent thyroiditis. I had one my sophomore year of high school and had to sit out the entire outdoor track season because of it. My resting heart rate was through the roof and my running took a nose dive. I was on beta blockers for a few weeks and within a few months my thyroid function decreased and I was put on Levoxyl. I've been on and off it for several years and it looks like I'll probably need take it for the rest of my life. I remember reading that Jeff See had a thyroiditis when he was in high school....

Sezzwho? wrote:

Correction T3 plays a role in EPO production.

We can not do much to really research that subject becuase there is no real studies that relate to it. Sure, some have concluded that it has something to do with natuaral EPO production. But to what point and how? I can tell you that if these guys have found a way to make their body produce extra EPO they could be VERY rich. THat could be a huge cancer treatment (as that is what the medical use is for EPO for the most part). I am sure natural EPO would be a much better thing to have.

Do you really think that these guys would waste this on having some guy run 27:30 for a 10k when lives are being lost? Let's hope not there buddy.

Great stuff Noname-I think my thyroid problem started from distance running years ago thanks.

Ghost of Brigham Young wrote:

That's fine, but don't tell me they don't help you run faster if you use them. They do.

no, they don't unless you need them. Sagarin nailed it with anemia. iron only helps people who are low in iron. If you take iron and don't need it to try and improve performance, you can end up with a disease called hemochromotosis, which can be deadly.

same goes for thyroid hormone, it only helps you if your body doesn't produce enough. if you take too much, you have hyperthryoidism.

I don't know about Thyroid meds, but does anyone else realize that Alot of Salazars athletes, once they arrive in OR, are sent to a doctor and "diagnosed" with exercise induced asthma and given a steroid inhalant. No rumor folks, i know of at least 4 of his athletes who have miraculously come down with asthma after years of running in other environments including high altitude. The air in Eugene must suck ;) i wish i knew a doctor to hook me up too.

[quote]noname wrote:

If you take iron and don't need it to try and improve performance, you can end up with a disease called hemochromotosis, which can be deadly.

[quote]

i need to correct this, you don't get hemochromatosis from taking too much iron. it's a disease where the body stores too much iron. but taking too much iron can cause some of the same problems.

They would not be very rich, plain ol' EPO and the like from AMGEN is much more effective. A method such as this is simply a back door quasi-legal way to boost the body's EPO much higher than by simply being exposed to altitude alone. It is the same "back door" quasi-legal technique that people use to claim "asthma" and can therefore get a waiver for an inhaler. An individual needs to be exposed to hypoxic conditions then given the proper dose of the correct thyroid med and the result is more EPO being produced than through simply being exposed to altitude alone. Placing cancer patients who are undergoing radiation or chemo into altitude tents to sleep then making them mildly hyperthyroid via thyroid meds seems like a bad idea, but that's just me. EPO from Amgen would be far more effective and would likely result in fewer malpractice suits.There are plenty of studies out there, all of this didn't just come out of my a$$, you just have to know what to look for and be able to understand the terminology.

cdavis wrote:

I can tell you that if these guys have found a way to make their body produce extra EPO they could be VERY rich. THat could be a huge cancer treatment (as that is what the medical use is for EPO for the most part). I am sure natural EPO would be a much better thing to have.

Kennedy never trained at altitude or had an altitude tent. Kinda kills your little theory in his case.

Salazar himself only found out he was hypothyroid when his running career was pretty much done.

I have no idea if Goucher has an altitude tent.

Lastly, as everyone pointed out, giving synthroid to someone who is not hypothyroid causes major problems. Yes, just being slightly hyperthyroid will severely mess up your running. Just ask any of those posters who are talking about regulating their medication.

Interesting...

i once wanted to be a subject in an exercise @ altitude study but hypothyroidism was one of the exclusion criteria. i asked the researcher why and he said hypothyroid people acclimitize differently than nomals...this was interesting to me cause i've been at altitude (14k+) several times and didn't have any unusal issues. so he sent me the following references. none of them were using hypothyroid subjects so i'm not sure if these are relevant. but i figured the more research is posted, the more likely it is someone out there with some knowledge will read it.

Connors, J. M. and L. G. Martin (1982). "Altitude-induced changes in plasma thyroxine, 3,5,3'-triiodothyronine, and thyrotropin in rats." J Appl Physiol 53(2): 313-5.

We have studied the thyroid function of high-altitude-acclimated (6,900 m for 5 wk) and nonaltitude-acclimated control (198 m) rats. After 5 wk of high-altitude exposure the plasma concentrations of both thyroxine (T4) and triiodothyronine (T3) were lower than those in control rats (4.7 +/- 0.3 vs. 3.3 +/- 0.2 microgram/dl and 96 +/- 5 vs. 74 +/- 6 ng/dl, respectively). The plasma thyrotropin (TSH) concentration was elevated in the high-altitude-acclimated rats compared with controls (52 +/- 4 vs. 29 +/- 3 micrograms/dl, respectively). Gross anatomical (thyroid wt/body wt) and histological observations of thyroid tissue were consistent with elevated plasma TSH concentrations. These results suggest that the fall in the plasma concentrations of T4 and T3 during acclimation to severe hypoxia is due to a primary block of thyroid secretion and not to a fall in plasma TSH levels.

Humpeler, E., F. Skrabal, et al. (1980). "Influence of exposure to moderate altitude on the plasma concentraton of cortisol, aldosterone, renin, testosterone, and gonadotropins." Eur J Appl Physiol Occup Physiol 45(2-3): 167-76.

The influence of 11 days at moderate altitude (2,000 m) combined with exercise on plasma concentration of testosterone, FSH (follicle-stimulating hormone), LH (luteinizing hormone), cortisol, aldosterone, and renin activity was studied in ten healthy subjects. Within 48 h of arrival at moderate altitude a significant increase in testosterone was found whereas FSH had decreased significantly and LH showed a tendency to decrease. Cortisol increased significantly at the beginning and reached a maximum at the end of altitude exposure. The plasma aldosterone level rose continuously and on the last day of altitude was significantly elevated. Plasma renin activity showed a tendency to decrease. On return to low land all measured parameters returned to base line values within 2 days. The findings of increases in plasma levels of aldosterone and testosterone (and serum T3 and T4, as reported by others) are in contrast to the previously found decrease of urinary excretion of all these hormones. This appears to be a distinct dissociation of serum levels of adrenal (and thyroid) hormones from their urinary excretion. The observed increase in plasma aldosterone is probably mediated through ACTH and the rise in plasma potassium, since plasma renin activity showed an opposite trend. The rise in plasma testosterone is probably of adrenal origin since plasma gonadotropins declined simultaneously. The increase of plasma levels of glucocorticoids, mineralocorticoids, and androgens after an ascent from 600 m to 2,000 m above sea level is compatible with an ACTH-mediated stimulation of the entire adrenal cortex and/or a diminished elimination of adrenal steroids: The concomitant fall of FSH, LH, and plasma renin would then be a consequence of a direct negative feedback inhibition of these hormones.

Loucks, A. B. and R. Callister (1993). "Induction and prevention of low-T3 syndrome in exercising women." Am J Physiol 264(5 Pt 2): R924-30.

To investigate the influence of exercise on thyroid metabolism, 46 healthy young regularly menstruating sedentary women were randomly assigned to a 3 x 2 experimental design of aerobic exercise and energy availability treatments. Energy availability was defined as dietary energy intake minus energy expenditure during exercise. After 4 days of treatments, low energy availability (8 vs. 30 kcal.kg body wt-1.day-1) had reduced 3,5,3'-triiodothyronine (T3) by 15% and free T3 (fT3) by 18% and had increased thyroxine (T4) by 7% and reverse T3 (rT3) by 24% (all P `` 0.01), whereas free T4 (fT4) was unchanged (P = 0.08). Exercise quantity (0 vs. 1,300 kcal/day) and intensity (40 vs. 70% of aerobic capacity) did not affect any thyroid hormone (all P %% 0.10). That is, low-T3 syndrome was induced by the energy cost of exercise and was prevented in exercising women by increasing dietary energy intake. Selective observation of low-T3 syndrome in amenorrheic and not in regularly menstruating athletes suggests that exercise may compromise the availability of energy for reproductive function in humans. If so, athletic amenorrhea might be prevented or reversed through dietary reform without reducing exercise quantity or intensity.

Mordes, J. P., F. D. Blume, et al. (1983). "High-altitude pituitary-thyroid dysfunction on Mount Everest." N Engl J Med 308(19): 1135-8.

(No abstract available)

No one has questioned the ethics of going to altitude. But many athletes could not afford to take time off work or leave family commitments to undertake altitude training. There are also athletes who do take performance enhancing substances that increase red blood cell mass. Our company is able to level the playing field - ensuring that 'legal' performance enhancements are available to all. A large number of athletes and sports teams across the world are using our systems; George Hincapie, Tim DeBoom, Peter Reid, Ed Moses, Bob Kennedy... The list is long and these world leaders are all happy to state that they utilise our Altitude Simulation system.http://www.altitudetent.co.uk/

unknowingly wrote:

Kennedy never trained at altitude or had an altitude tent. Kinda kills your little theory in his case.

Some more tidbits

HORMONE & GLUCOSE IMPACT EPO LEVELS

EPO production also has hormonal-dependant roots complexly related to glucose

metabolism, and calorie adequacy. The effect of Thyroid-T3 replacement and

glucose supplementation on erythropoietin production was investigated in fasted

hypoxic rats. It was found that 48 hr of fasting significantly reduced the circulating

levels of thyroid hormones and the production of renal and extrarenal

erythropoietin in response to hypoxia. These effects of fasting were completely

abolished when the animals had free access to 25% glucose solution as drinking

water, despite their lack of protein intake. Replacement doses of T3 (0.5

micrograms/100 gm per day) restored erythropoietin production in the fasted

animals but also increased the response of the fed controls. To avoid the effect of

endogenous T3, the experiments were repeated in thyroidectomized rats.

The thryroid medication has nothing to do with thyroid problems. It is a masking agent. I have second hand knowledge of one of the nike runners who dropped off the map. The reason he did was because he quit because he didn't want to go down the drug path which was obviously an option/norm at nike.

Time course of erythropoietin, triiodothyronine, thyroxine, and thyroid-stimulating hormone at 2,315 m.

Physiologisches Institut, Freie Universitat Berlin, Germany.

Erythropoietin (EPO), triiodothyronine, thyroxine, thyroid-stimulating hormone (TSH), hemoglobin (Hb), reticulocytes, packed cell volume, and plasma volume changes were studied in 29 male Austrian mountain rescue soldiers before and several days after an ascent from 744 to 2,315 m in the Alps. EPO concentrations showed a remarkable increase 48 h after the ascent (P < 0.01). No significant changes were found in triiodothyronine, thyroxine, and TSH. Reticulocytes increased only slightly. Hb decreased during the week (P < 0.01). Packed cell volume did not change, whereas plasma volume showed a slight decrease for 48 h after the ascent but then increased constantly (P < 0.01). It seems that thyroid hormones, TSH, and Hb play only a minor role in the regulation of EPO production and release under mild hypobaric-hypoxic conditions (2,315 m).